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SASH1 acts through NOTCH1 (show NOTCH1 ELISA Kits) and its inhibitor DLK1 (show DLK1 ELISA Kits) in a three-dimensional model of lumenogenesis involving CEACAM1 (show CEACAM1 ELISA Kits).
The data presented in this work suggest that a fine regulation of NOTCH (show NOTCH1 ELISA Kits) signaling BY DLK1 (show DLK1 ELISA Kits) plays an important role in the control of breast cancer cell proliferation and invasion.
results demonstrate that miR (show MLXIP ELISA Kits)-129-5p inhibits non-small cell lung cancer stemness and chemoresistance through direct targeting of DLK1 (show DLK1 ELISA Kits)
A complex defect of DLK1 (show DLK1 ELISA Kits) ( approximately 14-kb deletion and 269-bp duplication) was identified in a family with central precocious puberty. This deletion included the 5' untranslated region and the first exon of DLK1 (show DLK1 ELISA Kits), including the translational start site. Only family members who inherited the defect from their father have precocious puberty, consistent with the known imprinting of DLK1 (show DLK1 ELISA Kits).
Loss of DLK1 (show DLK1 ELISA Kits) expression is associated with fetal growth retardation complications of pregnancy.
LZK (show MAP3K13 ELISA Kits) cooperates with DLK (show DAPK3 ELISA Kits) to promote retinal ganglion cell death in response to axon injury.
In neonatal skin, DLK1 (show DLK1 ELISA Kits) exhibited a high degree of monoallelic expression from the paternal allele.
The study evaluated the roles of extracellular soluble DLK1 (show DLK1 ELISA Kits), comprising six EGF (show EGF ELISA Kits)-like domains and juxtamembrane regions, in human pancreatic cancer MIA (show MIA ELISA Kits) PaCa-2 cells in vitro and in vivo. Soluble DLK1 (show DLK1 ELISA Kits) exerted antitumor effects not only in cancer cell migration and anchorage-independent cell growth but also in in vivo tumor growth.
Treatment of mice with recombinant human DLK1 (show DLK1 ELISA Kits) during pregnancy has significant effects on AT of the offspring. This can be associated with counter-regulatory changes in the Notch1 (show NOTCH1 ELISA Kits) signaling cascade.
NOTCH1 (show NOTCH1 ELISA Kits) ligand Delta-like 1 (show DLL1 ELISA Kits) homolog (DLK1 (show DLK1 ELISA Kits)) self interacts
Results provide the first evidence that axon guidance genes are downstream targets of the dual leucine zipper kinase (DLK) signaling pathway, which through their regulation probably modulates neuronal cell development, structure and function.
the prevention of the nuclear localization of DLK (show DAPK3 ELISA Kits) as induced by prediabetic signals with consecutive suppression of beta-cell apoptosis might constitute a novel target in the therapy of diabetes mellitus
Data assesses DLK's role in axons of adult, injured CNS neurons in vivo and shows that DLK (show DAPK3 ELISA Kits) does not appear to have a critical function in axonal degeneration; function appears restricted to soma
This study provides compelling evidence for the pivotal roles of the ZPK/DLK and MKK4/MAP2K4 (show MAP2K4 ELISA Kits)-dependent mechanism in axotomy-induced motoneuron death in neonates
DLK (show DAPK3 ELISA Kits)-inducible knockouts displayed a modest increase in basal synaptic transmission but had an attenuation of the JNK/c-Jun stress response pathway activation and significantly reduced neuronal degeneration after kainic acid-induced seizures.
Abundance of DLK (show DAPK3 ELISA Kits) in turn controlled the levels of downstream JNK (show MAPK8 ELISA Kits) signaling and apoptosis.
DLK (show DAPK3 ELISA Kits) is required for RGC JNK (show MAPK8 ELISA Kits) activation and cell death in a rodent model of optic neuropathy
The cell intrinsic factors that determine whether a neuron regenerates or undergoes apoptosis in response to axonal injury are not well defined. DLK (show DAPK3 ELISA Kits) is an essential upstream mediator of both of these divergent outcomes in the same cell type.
These data demonstrate that DLK (show DAPK3 ELISA Kits) enhances regeneration by promoting a retrograde injury signal that is required for the activation of the neuronal proregenerative program.
This gene encodes a member of the serine/threonine protein kinase family. This kinase contains a leucine-zipper domain and is predominately expressed in neuronal cells. The phosphorylation state of this kinase in synaptic terminals was shown to be regulated by membrane depolarization via calcineurin. This kinase forms heterodimers with leucine zipper containing transcription factors, such as cAMP responsive element binding protein (CREB) and MYC, and thus may play a regulatory role in PKA or retinoic acid induced neuronal differentiation. Alternatively spliced transcript variants encoding different proteins have been described.
, dual leucine zipper bearing kinase
, dual leucine zipper kinase DLK
, leucine zipper protein kinase
, mixed lineage kinase
, protein kinase MUK
, Mitogen activated protein kinase 12 (Zipper (leucine) protein kinase)
, Zipper (leucine) protein kinase
, dual leucine zipper kinase
, leucine-zipper protein kinase
, mitogen-activated protein kinase kinase kinase 12
, mitogen activated protein kinase kinase kinase 12
, zipper (leucine) protein kinase
, mitogen activated protein kinase kinase kinase 12 type A
, mitogen activated protein kinase kinase kinase 12 type B
, mitogen-activated protein kinase kinase kinase 12 L homeolog